Man develops hypoxic pulmonary hypertension at high altitudes and in association with a number of heart and lung diseases. Many animals also develop this disorder of which cattle are particularly susceptible. Cattle maintained at high altitudes often show severe hypoxic pulmonary hypertension with right heart failure, a condition known as brisket disease. We found in early studies that some cattle were more susceptible to brisket disease than others even within the same breed. This encouraged us to undertake a breeding program which ultimately led to the development of susceptible and resistant strains of Hereford cattle for use as models in studies of hypoxic pulmonary hypertension. A similar program is being conducted in miniature swine to develop an alternate animal model. Our studies have shown that in cattle the traits of susceptibility and resistance to hypoxic pulmonary hypertension are transmitted from parents to offspring. Further, at ages 2-4 months susceptible calves (compared to resistant calves) have hypertrophied pulmonary arterioles, show greater pulmonary pressor responses to hypoxia and vasoactive substances, have "blunted" ventilatory responses to acute hypoxia and hypercapnia, and generally show, with acute and chronic hypoxic exposures, lower arterial O2 tensions, higher arterial CO2 tensions and higher hematocrit, hemoglobin and erythropoietin levels. These results have raised several questions. Are the traits of susceptibility and resistance to hypoxic pulmonary hypertension in cattle genetically transmitted or acquired? We hope to answer this question by conducting embryo transfers from susceptible and resistant cows to ordinary recipient cows. If the resultant progeny are found to be susceptible and resistant like their respective "true" mothers the traits must be genetically determined but if not, they must be acquired. If acquired are the characteristics of pulmonary vascular hypertrophy and augmented pulmonary pressor responses in the susceptible cattle developed in utero or postnatally? If present only after birth are these characteristics merely the result of a "blunted" hypoxic ventilatory drive which might be either inherited or acquired? We propose to answer some of those questions by examining the structure and function of the pulmonary vascular systems of susceptible and resistant calves during their fetal and early postnatal periods. Ventilatory responses to hypo (Text Truncated - Exceeds Capacity)